1. Field of the Invention
The present invention relates generally to tissue treatment systems and in particular to methods for stimulating cartilage formation.
2. Description of Related Art
Clinical studies and practice have shown that providing a reduced pressure in proximity to a tissue site augments and accelerates the growth of new tissue at the tissue site. The applications of this phenomenon are numerous, but application of reduced pressure has been particularly successful in treating wounds. This treatment (frequently referred to in the medical community as “negative pressure wound therapy,” “reduced pressure therapy,” or “vacuum therapy”) provides a number of benefits, including faster healing and increased formulation of granulation tissue. Typically, reduced pressure is applied to tissue through a porous pad or other manifolding device. Unless otherwise indicated, as used herein, “or” does not require mutual exclusivity. The porous pad, often an open-cell foam, contains cells or pores that are capable of distributing reduced pressure to the tissue and channeling fluids that are drawn from the tissue. The porous pad is generally sized to fit the existing wound, placed in contact with the wound, and then periodically replaced with smaller pieces of foam as the wound begins to heal and becomes smaller. The porous pad often is incorporated into a dressing having other components that facilitate treatment. While reduced pressure therapy has been used to treat soft tissue injuries, it has not been used to promote, for example, cartilage regeneration.
Damage to cartilage through age, injury, wear and metabolic disorders, such as osteoarthritis, affect millions of people throughout the world. Indeed, it is currently believed that 85% of all Americans will develop degenerative joint disease as a result of normal activities that damage cartilage. The gradual degeneration and destruction of articular cartilage may be due to trauma, structural deformation of the joints and being overweight. The process thins the cartilage, in part through programmed cell death, or apoptosis. The clinical manifestations of cartilage damage or wear are often painful and debilitating, including swelling of the joint, crepitation, and decrease in functional mobility. As the condition worsens, pain may even limit minimum physical efforts and persist at rest making it difficult to sleep. If the condition persists without correction and/or therapy, the joint can be totally destroyed, leading the patient to major replacement surgery with a total prosthesis, or to disability. The complications of cartilage injury are multifold. For example, injured cartilage tends to cause additional damage to articulations and the articular surfaces. Damage to articular surfaces is linked to bone spur development, which further limits joint movement.
Moreover, cartilage is the main structural support of various parts of the body, such as ears and the nose. As such, a lack of cartilage from injury may also result in a cosmetic defect. Thus, in sum, damaged and degraded cartilage results in a reduced quality of life.
The body, however, cannot completely repair the cartilage. Cartilage is primarily composed of collagen fibers, proteoglycans and elastin fibers that form an extracellular matrix. The matrix is formed by specialized cells called chondrocytes. Chondrocytes are one of the few cell types that can survive with a minimal blood supply. However, when cartilage is damaged, the lack of an adequate blood supply to the chondrocytes results in an inability to regenerate new chondrocytes, a process that requires an increased amount of nutrients and access through the blood stream to other cells and proteins. Full thickness articular cartilage damage or osteochondral lesions may allow for normal inflammatory response, but then result in repair with functionally inferior fibrocartilage formation.
Current techniques to inhibit or delay degeneration of joint cartilage include use of anti-inflammatory agents, chondrogenic stimulating factors, antirheumatics, systemics, viscoprotection and injection of depot steroids. Other methods include implantation of chondrocytes or synthetic matrices. One method of treatment for cartilage damage is surgical intervention, with reattachment and reconstruction of the damaged tissue. None of the above methods are totally satisfactory, and those methods rarely restore full function or return the tissue to its native normal state. In addition, none of those methods are proven to regenerate cartilage in situ and in vivo.
Further, there is no proven way to promote healing of dense connective tissue structures such as ligaments and tendons. Ligament and tendon injuries are commonplace and difficult to heal. Indeed, it is not uncommon to repair complete ruptures or tears of a ligament or tendon by immediate surgery to remove the damaged tissue and replace it with a graft. Post surgery, a graft recipient has to experience the long task of rehabilitation and healing. It is often difficult to repair ligaments and tendons by current methods. Thus, when repair is an option, the joints and muscles attached to the ligament or tendon are often immobilized to enable the tissue to heal.
As such, there is currently an acute need for a safe, simple, rapid, inexpensive and efficient system and method for regenerating connective tissues in areas where the connective tissue is missing, damaged, or worn.